DESCRIPTION One of the risk factors for essential hypertension is salt-sensitivity ; however, the metabolic, cellular, and molecular mechanisms involved in increased pressor response to Na-loading are not known. Metabolic and genetic studies of the causes of salt-sensitivity should be especially fruitful in normotensive and hypertensive African-Americans because they have a higher prevalence of salt-sensitivity . Altered Na homeostasis is marked by increased intracellular Na (Na-i) levels, depressed Rb+ uptake and depressed Na pump activity and these may be important phenotypic markers for salt-sensitive hypertension. Because eicosanoid products of cytochrome P450-dependent arachidonic acid metabolism inhibit Na pump activity, these products may also be important markers of hypertension. In addition, based on reports in the literature, polymorphisms of the alpha-1 Na,K-ATPase (Na pump) and the Type 1 amiloride sensitive Na channel loci may affect hypertension. The current proposal will extend ongoing studies in African-Americans in Cleveland to a Ugandan population. Prevalence of hypertension will be estimated, as well as the relationship between hypertension, environmental risk factors, intermediate phenotypes (for example, Na-i and cytochrome P450-dependent arachidonic acid metabolites), and genotypes at the two candidate loci.